Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum vitamin A, vitamin E, vitamin B12, folate and leucocyte vitamin C were measured in 45 patients between the ages of one month and 2 1/2 years who were receiving total parenteral nutrition. After allowing for variations in intake the following recommendations are made: Vitamin A (central vein) 2,500 i.u./day (peripheral vein) 1,000 - 1,500 i.u./day. Vitamin E (peripheral vein) 0.8 mg/kg/day, Vitamin B12 (central vein) 0.8 - 1 microgram/day, Folate (central vein) 10 - 80 microgram/day, Vitamin C (central vein) 25 mg/day.
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PMID:[Supply of vitamin A, E, C, B 12 and folates during total parenteral nutrition in pediatrics]. 10 63

The effect of vitamin A, a membrane surface-active agent, on parathyroid hormone secretion was studied in vitro, using bovine parathyroid tissue, and in vivo in man. Parathyroid tissues were incubated with vitamin A (retinol), retinoic acid, and calcium, and with hydrocortisone and vitamin E, agents that antagonize the membrane effects of vitamin A. The stimulation of parathyroid hormone release by vitamin A, 10(-6) to 10(-9) mol/1 in vitro, was dose and time dependent. Retinoic acid did not stimulate secretion. High calcium concentration, hydrocortisone, 10(-5) mol/1 and 10(-6) mol/1, and vitamin E, 10(-5) mol/1, antagonized vitamin A-induced parathyroid hormone secretion. Vitamin A increased the lysosomal cathepsin D activity of parathyroid tissues. In human studies, eleven healthy men received two intramuscular injections of vitamin A palmitate, 25 000 units each, within 24 h. In every subject, serum parathyroid hormone increased after vitamin A administration. Our studies indicate that: (1) vitamin A stimulates parathyroid hormone secretion in vitro, possibly through modification of the cell or secretion granule membrane, or through stimulation of lysosomal proteolytic activity, and (2) vitamin A increases serum parathyroid hormone in vivo, and this effect may be important in clinical states of vitamin A excess.
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PMID:Vitamin A stimulation of parathyroid hormone: interactions with calcium, hydrocortisone, and vitamin E in bovine parathyroid tissues and effects of vitamin A in man. 40 51

To investigate the role of normal vitamin E levels and the interrelationships between vitamin E and A in maintaining the visual cells of the retina, weanling female Sprague-Dawley rats were fed vitamin E-free diets differing tenfold in their vitamin A content (0.8 and 8.0 mg of retinol per kilogram of diet). Rats on vitamin E-free diets with the higher vitamin A level exhibited marked disruption of photoreceptor outer segment membranes and a fivefold increase in the number of lipofuscin granules in the pigment epithelial cells which ingest these membranes. Rats on vitamin E-free diets with the lower vitamin A level showed the same retinal damages plus significant loss of photoreceptor cells compared to age-matched rats on control diets. Rods and cones were involved equally, and their pattern of loss was not like that found in vitamin A deficiency. Normal levels of vitamin E probably protect photoreceptor membranes from oxidative damage and retard the accumulation of their remnants and other products of lipid breakdown in the pigment epithelium. The vitamin A status of rats has a significant influence on the extent of damage induced by vitamin E deficiency.
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PMID:Vitamin E deficiency and the retina: photoreceptor and pigment epithelial changes. 44 67

This paper describes a rapid, microprocedure for the simultaneous determination of alpha-tocopherol (vitamin E) and retinol (vitamin A) in plasma, and of alpha-tocopherol alone in red cells since cells do not contain retinol. A total lipid extract from 0.1 ml plasma or 0.125 ml red cells and containing internal standards of alpha-tocopheryl acetate and retinyl acetates is injected onto a high pressure liquid chromatography with a reverse phase column developed with methanol-water. An ultraviolet detector with 280-nm filter is used. The chromatogram is complete in 8 min and the alpha-tocopherol and retinol are quantitated by the peak height ratio method. Comparison of results with both plasma and red cells gave excellent agreement with conventional methods for these vitamins. The procedure should be particularly useful for clinical studies and nutrition surveys.
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PMID:Simultaneous determination of alpha-tocopherol and retinol in plasma or red cells by high pressure liquid chromatography. 48 33

Erythrocytes from rats fed large doses of Vitamin A alone, or large doses of vitamin A and vitamin E or diphenyl-p-phenylene diamine (DPPD) were studied for H2O2-induced hemolysis. The vitamin A-dosed rats were more susceptible than normal rats to H2O2-induced hemolysis. Hemolysis was not accompanied by lipid peroxidation. Nevertheless, the antioxidants vitamin E and DPPD inhibited hemolysis in erythrocytes from vitamin A-dosed rats. These antioxidants had the same inhibitory effect when they were included in the diet or added to erythrocyte suspensions in vitro. Erythrocytes from vitamin A-dosed rats with or without added vitamin E or DPPD were less susceptible than the erythrocytes from normal rats to osmotic challenge, showing that vitamin A was present in levels sufficient to alter the structure of the erythrocyte membrane. These studies show that oxidative hemolysis occurs when the erythrocyte membrane is modified. Furthermore, this oxidative hemolysis is unrelated to lipid peroxidation.
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PMID:Effect of hypervitaminosis A on hemolysis and lipid peroxidation in the rat. 65 91

Male Holtzman rats (78 g) were fed semipurified 16% protein diets for 8 weeks using a food grade soy protein concentrate as the protein source. The basal diet (A) contained added DL-methionine (0.26%) and adequate amounts of vitamins A (14,535 IU/kg as retinyl acetate) and E (60 IU/kg as DL-alpha-tocopheryl acetate) and all other required nutrients. Experimental diets included: (B) basal plus 600 IU of vitamin E/kg; (C) basal plus 6,000 IU of vitamin E/kg; (D) basal plus 2.9 X 10(6) IU of vitamin A/kg; (E) basal plus 2.9 X 10(6) IU of vitamin A plus 600 IU of vitamin E/kg; and (F) basal plus 2.9 X 10(6) IU of vitamin A plus 6,000 IU of vitamin E/kg. Both vitamin A and vitamin E had a significant (P less than 0.05) effect on growth. There was an increase in growth with vitamin E intake and a decrease in growth with vitamin A intake. The net result of these two effects was that the groups fed both vitamins tended to be quite close in mean values to the group fed only the basal diet. Vitamin A significantly (P less than 0.05) increased relative weights of spleen and testes; vitamin E reduced that effect. Vitamin E also significantly (P less than 0.05) reduced relative adrenal weight whereas vitamin A significantly increased it. The two effects tend to cancel each other in the sense that the group fed both vitamins had an average relative adrenal weight quite close to that of the group fed only the basal diet. However, vitamin A still had an effect even when 6,000 IU of vitamin E was fed. The interaction effect of the two vitamins was significant (P less than 0.05) for plasma total protein and liver vitamin A. There was an increase in liver vitamin A with increasing levels of vitamin E in the diet. Blood urea nitrogen and plasma cholesterol were unchanged. A significant interaction of vitamins A and E was found to effect plasma total protein, liver vitamin A, and relative weight of spleen and testes.
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PMID:Influence of excess vitamin E on vitamin A toxicity in rats. 123 14

We present the dietary epidemiology of bladder cancer while controlling for a number of lifestyle and environmental risk factors in a study of 351 white male cases with histologically confirmed transitional cell carcinoma of the bladder and 855 white male controls selected from Erie, Niagara, and Monroe counties of western New York from 1979 to 1985. Usual diet was estimated by comprehensive interviews with use of a detailed food frequency questionnaire. An increased risk of bladder cancer was associated with higher kilocalorie intake, but only among those under 65 years of age, with the strongest pattern associated with fat intake. Further analyses of fat, carbohydrates, and protein, with adjustment for total kilocalories, resulted in a positive association of risk with fat intake and a decreasing risk with higher protein intake. Of the vitamins, carotenoid consumption appeared to decrease risk with increased consumption for those under 65 years of age. No significant differences between cases and controls were seen for intake of calcium, retinol, thiamin, riboflavin, niacin, vitamin C, vitamin D, and vitamin E. After adjustment for kilocalories and other confounders, higher intake of dietary sodium was associated with increased risk among both age groups, and the trends were statistically significant. The importance of diet in the etiology of bladder cancer is suggested by our findings.
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PMID:Diet in the epidemiology of bladder cancer in western New York. 129 99

The present study report 7 cases of sickle homozygous disease which have been analysed using markers of the oxidative-stress, 26 african male subjects were studied: 7 Hb SS subjects (age: m = 20) and 19 control subjects (Hb AA, age: m = 40). Plasma concentrations of F-MDA, T-MDA, TBARS, alpha tocopherol, retinol and beta carotene were measured. Plasma MDA and TBARS mean levels increased in sickle homozygous patients more than in controls. However, only TBARS mean concentrations were significantly increased between patients and controls: TBARS: 4.14 +/- 1.49 nMol/ml for Hb SS versus 2.10 +/- 1.21 nMol/ml for Hb AA (P less than 0.005). Vitamin A and vitamin E concentrations were significantly lower in Hb SS than in Hb AA. Beta carotene was significantly increased in patients vs controls. The significant increase of TBARS explains the great importance of the oxidative damage, whereas the significant decrease of vitamins A and E, may contribute, at least for a part, to maintain the autoxidation process or reveals its intensity in these patients.
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PMID:[First observations on the main plasma parameters of oxidative stress in homozygous sickle cell disease]. 132 59

We conducted a prospective study of diet in relation to the incidence of basal cell carcinoma of the skin in a cohort of 73,366 women who were 34 to 59 years old in 1980 and without previous skin or other cancer. During 4 years of follow-up, 771 incident cases of basal cell carcinoma were diagnosed. When adjusted for other risk factors, women in the highest quintile of energy intake were at higher risk of basal cell carcinoma compared with those in the lowest quintile (relative risk, 1.28; 95% confidence interval, 1.02 to 1.60). No significant associations were observed between risk of basal cell carcinoma and energy-adjusted intake of dietary fat, carotenoids with vitamin A activity, and retinol, vitamin C, vitamin D, and vitamin E, either with or without supplements. Use of specific vitamin A, C, D, or E supplements, or multivitamins, did not materially alter risk. Although the period of follow-up was relatively short, these data are most consistent with no major role for these nutrients in the etiology of basal cell carcinoma.
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PMID:Diet and risk of basal cell carcinoma of the skin in a prospective cohort of women. 134 73

The effects of retinol and alpha-tocopherol-deficient and supplemented diets on the cytosolic concentration of thiobarbituric acid reactive substances (TBARS) in rat liver have been studied. Physiological lipoperoxidation (LPO) was observed in liver cytosol of control rats (TBARS = 0.315 +/- 0.034 nmol of MDA equivalents/mg of liver cytosolic proteins). In retinol-deficient diets there was a decrease in retinolaemia and the absence of retinol in liver cytosol while cytosolic TBARS increased significantly (P less than 0.001). Vitamin E was not found in cytosolic fractions, except in alpha-tocopherol-supplemented diet rats. alpha-Tocopherol-deficient diets induced an absence of vitamin E in the serum and cytosolic TBARS were increased compared to controls (P less than 0.001). Supplementation of the diet with retinol and alpha-tocopherol or both in combination induced a significant decrease in liver cytosolic TBARS (P less than 0.001). Finally the combination of low dietary supplementation with retinol and alpha-tocopherol (ten times the normal diet each) induced the maximum anti-LPO effect.
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PMID:Relationship between dietary retinol and alpha-tocopherol and lipid peroxidation in rat liver cytosol. 139 87


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